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Majid Almansouri Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Pooja Patel Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Janet Chamberlain Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK

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Sheila Francis Department of Infection Immunity and Cardiovascular Disease, University of Sheffield, Medical School, Sheffield, UK
Healthy Lifespan Institute HELSI, University of Sheffield, Medical School, Sheffield, UK

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oxidised low-density lipoprotein (oxLDL) which then accumulates inside cells ( 2 ) causing interleukin-1β (IL-1β) production and release ( 3 ). Experimental studies in animal models ( 4 ) and recent trials, e.g. CANTOS ( 5 ), have indicated that the IL-1β

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Isabelle Coornaert Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Annelies Breynaert NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Nina Hermans NatuRAPT Research Group, University of Antwerp, Antwerp, Belgium

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Guido R Y De Meyer Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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Wim Martinet Laboratory of Physiopharmacology, University of Antwerp, Antwerp, Belgium
Infla-Med Centre of Excellence, University of Antwerp, Antwerp, Belgium

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lipids, especially low-density lipoprotein (LDL) cholesterol, undergo oxidation, they become more prone to uptake by immune cells, triggering the inflammatory response within arterial walls ( 3 ). Oxidized LDL (oxLDL) contributes to the recruitment of

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Hafsa Khan International Centre for Chemical and Biological Sciences (ICCBS), Pakistan

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Tahira Ghulam Aga Khan University Medical College, Pakistan

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Naseer Ahmed Institute of Basic Medical Sciences, Khyber Medical University, Pakistan

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Muhammad Rafai Babar Aga Khan University Medical College, Pakistan

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Simon DJ Calaminus Hull York Medical School, University of Hull, UK

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Muhammad Zuhair Yusuf Aga Khan University Medical College, Pakistan

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( 12 , 13 ). Importantly in the presence of a prothrombotic environment, especially one with oxidized LDL (oxLDL), thrombus formation is excessive as the oxLDL helps to prevent the inhibition mediated by PGI 2 and NO, and therefore, the thrombus can

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Ka Ka Ting Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Paul Coleman Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Yang Zhao Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Mathew A Vadas Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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Jennifer R Gamble Centre for the Endothelium Vascular Biology Program Centenary Institute, The University of Sydney, Sydney, New South Wales, Australia

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-risk factors for atherosclerosis ( 68 ). Hypercholesterolemia is associated with increased blood levels of oxidized low-density lipoprotein (ox-LDL), well known to be involved in EC dysfunction and which induces EC senescence ( 69 , 70 ). Interestingly, the

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Sarah Costantino Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Shafeeq A Mohammed Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Samuele Ambrosini Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland

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Francesco Paneni Center for Molecular Cardiology, University of Zürich, Zürich, Switzerland
University Heart Center, Cardiology, University Hospital Zurich, Zürich, Switzerland
Department of Research and Education, University Hospital Zurich, Zürich, Switzerland

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high ox-LDL concentrations, RNCR3 depletion accelerated atherosclerosis, aggravated hypercholesterolemia and vascular inflammation while decreasing cell proliferation and migration ( 64 ). The lncRNA called myocardial infarction–associated transcript

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